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Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

ABSTRACT: Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

PROVIDER: PRJNA813877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18272158.fastq.gz	Fastqsanger.gz
	SRR18272159.fastq.gz	Fastqsanger.gz
	SRR18272160.fastq.gz	Fastqsanger.gz
	SRR18272161.fastq.gz	Fastqsanger.gz
	SRR18272162.fastq.gz	Fastqsanger.gz

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Similar Datasets

Cytosolic PRRs are required to upregulate inflammatory gene expression upon EZH2 inhibition with GSK343

2023-10-18 | GSE198159 | GEO

Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

Project description:EZH2 is a histone methyltransferase that deposits the repressive histone H3 lysine 27 trimethylation (H3K27me3). This mark has been reported to silence expression of various repetitive elements in the genome. We sought to identify the effect of EZH2 inhibition on coding and non-coding, repetitive RNA expression. We generated a novel mutant mouse line whose ability to detect induced repeat element expression has been abrogated. We report that the mutant splenic B cells fail to upregulate inflammatory gene expression upon EZH2 inhibition, despite comparable upregulation of various repetitive elements with WT. Unlike WT splenic B cells that do not upregulate interferon gene expression upon EZH2 inhibition, B16-F10 melanoma cells activate their expression under the same inhibitor treatment. Cytosolic pattern recognition receptors, RIG-I and Cgas, are required for such response as their deletion abrogates this pathway.

2023-10-18 | GSE239879 | GEO

Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

Project description:Cytosolic PRRs are required to upregulate interferon gene expression upon EZH2 inhibition with GSK343 in B16-F10 melanoma cells [RNA-seq]

| PRJNA1001317 | ENA

Treatment of CML CD34+ cells with EZH2 inhibitor GSK343

Project description:Transcriptional profiling by array of CML CD34+ cells to understand the response of chronic myeloid leukaemia stem cells to an EZH2 inhibitor, GSK343.

2016-11-01 | E-MTAB-2893 | biostudies-arrayexpress

Treatment of non-CML CD34+ cells with EZH2 inhibitor GSK343

Project description:Transcriptional profiling of non-CML CD34+ cells to understand the response of non-CML stem cells to an EZH2 inhibitor, GSK343.

2016-11-01 | E-MTAB-3552 | biostudies-arrayexpress

Inhibition of histone methyltransferase EZH2 in Schistosoma mansoni by GSK343 decreases the expression of genes implicated in DNA replication and ncRNA metabolism

Project description:Schistosomiasis is a chronic and debilitating disease caused by a trematode of the genus Schistosoma. The current strategy for the control of the disease involves treatment with Praziquantel, the only available drug. The development of new drugs is therefore a top priority. Drugs that inhibit histone modifying enzymes have been used in cancer, altering gene expression, replication, repair and DNA recombination. Schistosoma parasites have some characteristics similar to malignant tumors, such as intense cell division and high levels of metabolic activity. Here we evaluate in Schistosoma mansoni the effect of GSK343, an inhibitor of the histone methyltransferase EZH2 that had been shown to arrest or reduce the growth of human cancer cells. We show that GSK343 causes damage to the parasite tegument and reduces egg laying in vitro, concomitant with a decrease in levels of H3K27me3, the histone mark put in place by EZH2. RNA-seq and proteomic analyses of treated parasites showed changes in the expression of hundreds of genes involved in important metabolic processes. In females, a marked decrease was observed in the expression of genes related to processes such as DNA replication and noncoding RNA metabolism. In conclusion, the histone methyltransferase EZH2 seems to be a promising novel drug target against schistosomiasis.

2018-11-23 | PXD010342 | Pride

Study the differential gene expression of C57/BL6 Mouse tumors treated with EZH2 inhibitor GSK343 II

Project description:The study evaluated the differential gene expression in control Antibody or Ant-CXCL10 antibody injected mouse when compared to EZH2 inhibitor GSK343 treated mice tumors Briefly, control Antibody or Ant-CXCL10 antibody injected C57BL/6 mouse were treated with or without GSK343were analyzed for RNA-seq

2021-10-25 | GSE160176 | GEO

Gene regulation by EZH2 inhibitors

Project description:Our previous study has found that UNC1999 and GSK343 are potent autophagy inducers. To further investigate the underlying mechanisms, microarray analysis was performed. EZH2 inhibitor-induced gene expression in HCT116 was measured at 4 hours after exposure to 5 uM UNC1999 or 10 uM GSK343.

2016-06-23 | E-GEOD-83633 | biostudies-arrayexpress

PolyA RNA-seq from retinoic acid-differentiated iPSCs treated with GSK343, 5-aza, or Combo (GSK343 & 5-aza)

Project description:Analysis of steady-state mRNA levels in induced pluripotent stem cells (iPSCs) differentiated for 5 days with retinoic acid (RA) and treated for final 48 hrs with GSK343 (EZH2 inhibitor), 5-azacytidine (5-aza, DNA methyltransferase inhibitor), or their combination (Combo).

2022-11-08 | GSE207375 | GEO

Gene expression profiles of H16N2 cells expressing EZH2 variants

Project description:A cytosolic role for EZH2 in regulating cell signaling via interaction with the VAV family of proteins has been reported by us previously. However, it is unclear whether EZH2 interactions with VAV are critical for tumorigenesis. Here, we show that cytosolic EZH2 exhibits greater transforming/metastatic capacity than wild-type EZH2 and that targeted disruption of the EZH2-VAV interaction abolishes EZH2-promoted tumorigenesis. We also found that interaction of cytosolic EZH2 with VAV is critical for EZH2-mediated talin methylation and subsequent STAT3 activation. Both cytosolic EZH2 and a methyl-mimicking talin mutant substantially promoted STAT3 activation and tumor growth. We therefore propose that the VAV-dependent cytosolic function of EZH2 may be a critical step in the initiation of cellular transformation, preceding the well-established function of EZH2 in epigenetic silencing of tumor suppressors. Thus, disrupting EZH2-VAV interaction could be an alternative intervention strategy for treatment of cancers associated with EZH2 overexpression.

2017-10-04 | E-MTAB-3599 | biostudies-arrayexpress

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